CE Article: COPD Exacerbation

Objectives

• Identify the most common cause of exacerbation of COPD.

• Given a patient scenario, differentiate between exacerbation of COPD, acute decompensated heart failure, pulmonary embolism, pneumonia and pneumothorax as the cause of a patient’s respiratory distress.

• List the signs and symptoms associated with exacerbation of COPD.

• Describe the treatment for exacerbation of COPD.

Chronic obstructive pulmonary disease, or COPD, is a term that refers to a spectrum of diseases that result in restrictions in pulmonary airflow and breathing-related problems. The Global Initiative for Chronic Obstructive Lung Disease (GOLD)¹ defines COPD as being “characterized by persistent airflow limitation that is usually progressive and associated with an enhanced chronic inflammatory response in the airways and the lung to noxious particles or gases. Exacerbations and comorbidities contribute to the overall severity in individual patients.”

Specific diseases that contribute to COPD include emphysema, chronic bronchitis and chronic obstructive asthma. Definitions of COPD often emphasize emphysema and chronic bronchitis when describing the disease, and asthma has traditionally been left out of the spectrum. However, there are patients with asthma whose airflow obstruction does not completely improve between exacerbations. These patients are considered to have COPD. Comorbidities linked to COPD include hypertension, coronary artery disease, stroke, heart failure, diabetes mellitus, renal insufficiency, osteoporosis, depression and anxiety.²

COPD was the third-leading cause of death in the U.S. in 2011 and is expected to become the third-leading cause of death worldwide by 2020.^3,4 In 2011, the last year for which data is available, 15 million people in the U.S. reported they’d been diagnosed with COPD.⁵ The actual number is probably much higher, as the disease is both underrecognized and underdiagnosed.⁶ In the United Sates, exposure to tobacco smoke is the most common cause of COPD, though exposure to air pollutants in the workplace and home, genetic factors and respiratory infections also contribute.⁷

This month’s CE article uses three case scenarios to explore the evaluation and treatment of the patient with an exacerbation of COPD. These cases explore the clinical context of the elements of the history and clinical exam to form a “big picture” understanding of the event, and also discuss the appropriate management of the patient with COPD exacerbation in the prehospital setting.

Case #1

A 68-year-old female sits at her kitchen table, conscious, alert and oriented times four, in no apparent distress, but says, “I feel like I can’t catch my breath.” You note she’s on home oxygen via nasal cannula. She says she woke this morning feeling fine but experienced increasing dyspnea over the past six hours that’s unrelieved with use of her metered-dose inhalers (MDIs). When asked specifically, she says her dyspnea gets worse with exertion, but she feels “almost normal” when sitting down. She says she’s not had any recent respiratory problems or other illness. She denies any chest pain or discomfort, nausea or vomiting, dizziness, weakness, syncope or abdominal, head or back pain. She has a past medical history significant for COPD and hypertension; she does not presently smoke but was a 40-pack-a-year smoker prior to her diagnosis of COPD two years ago.

Regarding her COPD history, she says since being diagnosed and prescribed her MDIs two years ago, she has not had an exacerbation, a COPD-related visit to the emergency department or hospitalization. Her medications include Ventolin MDI prn; Atrovent MDI prn; Tudorza Pressair MDI bis; diltiazem; and oxygen via nasal cannula at 1 lpm. You note the patient does not seem anxious, sits upright but isn’t tripoding, can speak in 5–6-word sentences, and has no pursed-lipped breathing. Your clinical exam reveals no accessory muscle use, and her lungs have slight and diffuse expiratory wheezing in all fields with good air movement from the apices to bases bilaterally. You note there is no jugular venous distention and no edema in her ankles. Her vital signs are HR, 82/min. and irregular; BP, 122/70 mmHg; RR, 18/min. with good tidal volume; SpO₂, 92% on room air; EtCO₂, 58 mmHg. When you comment on the patient’s SpO₂ reading, she tells you it’s normal for her, adding “I have one of those little finger pulse oximeters and use it all the time to monitor myself.” A 12-lead ECG shows atrial fibrillation with no acute ST-segment or T-wave changes.

What is your differential diagnosis? What are the important clinical and historical findings? How would you manage this patient?

Discussion

The differential diagnosis for a patient with suspected COPD exacerbation should also include acute decompensated heart failure, pulmonary embolism, pneumonia and pneumothorax.⁸ This patient does not have a history of heart failure, is not presenting with evidence of decreased cardiac output (hypotension, tachycardia) and lacks any clinical findings that suggest left-sided (pulmonary edema) or right-sided (JVD, peripheral edema) heart failure. All of this makes acute heart failure unlikely. Likewise, pneumonia seems unlikely, as the patient describes no symptoms that suggest focal infection, history of recent respiratory infection, malaise, fever or other HPI components we’d expect with pneumonia.

Spontaneous pneumothorax is certainly a possibility, especially in a patient with COPD. Specifically, a secondary spontaneous pneumothorax is one that occurs secondary to underlying chronic lung disease. Patients with COPD are at risk of pneumothorax because of increased intrathoracic pressure, with rupture of apical blebs (see sidebar) being the most common cause.

COPD is the most common cause of spontaneous pneumothorax; anywhere from 50%–70% of all spontaneous pneumothoraces occur secondary to COPD.⁹ The clinical presentation of an SSP or any pneumothorax depends on the volume of air that escapes into the pleural space, the rate at which it progresses and the patient’s respiratory reserve. A small pneumothorax can be difficult to detect on clinical exam, as diminished lung sounds may not be discernible, especially in the often-noisy prehospital environment. The patient, however, does not present with pleuritic chest pain, tachycardia or any lowering of her baseline SpO₂, which we’d expect with even a small pneumothorax, as the typical patient with COPD will most likely have a decreased respiratory reserve and be unable to effectively compensate for a pneumothorax.

Pulmonary embolism (PE) is a possibility in this patient. Like pneumothorax, it can be difficult to identify in the prehospital environment, as its clinical manifestations can vary from no symptoms to obstructive shock and sudden death. In this stable patient, with no tachycardia and an SpO₂ at her normal baseline, it would be hard to argue for PE as the primary cause of her dyspnea. This leaves exacerbation of her COPD as the most likely culprit. An exacerbation of COPD is defined as an acute worsening of a patient’s respiratory symptoms from their day-to-day baseline that leads to a change in medications.¹ An exacerbation generally leads to a change in one or more of the cardinal symptoms associated with COPD:

• Increased dyspnea;

• Increased frequency and severity of cough;

• Increased sputum production and/or changes in character.

This argument is strengthened by the presence of wheezing and exertional dyspnea unrelieved with increased use of her short-acting MDIs.

The patient’s medications offer a glimpse into the severity of her disease. Note she’s prescribed a short-acting beta-2 agonist, Ventolin (albuterol), and a short-acting anticholenergic, Atrovent (ipratropium), as well as a long-acting anticholinergic, Tudorza Pressair (aclidinium). This combination of short-acting bronchodilators used when needed as well as regular treatment with a long-acting bronchodilator indicates she’s considered low-risk for exacerbations, yet is more symptomatic than others in this low-risk category at baseline in the GOLD Therapy by Disease Category Severity recommendations.¹

Prehospital management of the patient with COPD exacerbation includes reversing airflow limitation with short-acting bronchodilators, ensuring adequate oxygenation and ventilation, and averting intubation and mechanical ventilation. Arguably, all patients with exacerbation of COPD should have intravenous access established, be placed on a cardiac monitor, and receive a 12-lead ECG.

Administration of supplemental oxygen is a critical component of the prehospital management of COPD. There is, however, the well-known risk of worsened hypercapnea (elevated CO₂ levels in the blood) with excess oxygenation in COPD patients. Excessive oxygenation is bad, not oxygen. Current standards recommend supplemental oxygen be administered with a target SpO₂ of 88%–92%. This corresponds with a PaO₂ (arterial oxygen tension) of about 60–70 mmHg. In two randomized clinical trials, one performed in the prehospital setting, titrating supplemental oxygen to an endpoint of 88%–92% resulted in a lower mortality compared to the administration of high-flow oxygen.^10,11

Following these guidelines, the patient in this case should have her home oxygen rate of 1 lpm via nasal cannula continued during transport, as this flow rate is sufficient to produce a current SpO₂ of 90%. A nasal cannula can provide a fraction of inspired oxygen (FiO₂) up to 40% at a flow rate of 6 lpm. If a higher FiO₂ is required, the use of a simple facemask can in theory deliver an FiO₂ of up to 55% under near-perfect conditions, which do not always exist. The use of a nonrebreather mask with a tight face seal can also in theory deliver an FiO₂ of up to 90%, though this is seldom required in the patient with COPD. Venturi masks allow for the administration of a specific FiO₂ (24%, 28%, 31%, 35%, 40% or 60%) depending on the jet used.

Inhaled short-acting beta agonists (Table 1) are the backbone of prehospital patient management in exacerbation of COPD because of their rapid onset of action and effectiveness at reversing bronchoconstriction.⁸ The GOLD report recommends albuterol, fenoterol or levalbuterol diluted in normal saline and administered via nebulizer. The use of subcutaneous short-acting injectable or parenteral beta agonists such as epinephrine or terbutaline is not recommended in exacerbation of COPD because of their significant inotropic and chronotropic effects, which increase the risk of myocardial ischemia and cardiac dysrhythmia. Ipratroprium and oxitropium are common short-acting anticholinergic agents used in the management of COPD exacerbation. Anticholinergics dry respiratory secretions, the overproduction of which is a problem in COPD patients. They also act as agonists at acetylcholine receptors, increasing the effects of the parasympathetic nervous system and resulting in bronchodilation.

Although the use of a nebulized short-acting beta agonist (albuterol) in combination with a short-acting anticholinergic agent (ipratropium) is ubiquitous in both the prehospital and hospital settings, there is conflicting evidence regarding its efficacy.¹ The problem in the prehospital environment is that nebulizers are typically used utilizing 100% oxygen to supply the required airflow to aerosolize the medication, resulting in overoxygenation and the hazards associated with it. British Thoracic Society guidelines for use of oxygen in adult patients recommend using room air rather than oxygen to power nebulizers during medication administration, giving oxygen concurrently via nasal cannula at a flow rate sufficient to maintain saturation of 88%–92%. If use of room air is not possible, the BTS recommends limiting oxygen-driven nebulizer treatments to six minutes.¹²

The long-term use of oral corticosteroids has well-known and numerous undesirable side effects, perhaps the most important being immunosuppression. However, the short-term use of oral glucocorticoids in combination with inhaled/nebulized bronchodilators has been shown to improve the symptoms and decrease in lung function associated with exacerbation of COPD, as well as decrease hospital stay length. Corticosteroids administered orally absorb rapidly and reach peak serum levels in about one hour. IV corticosteroids can be used in patients with previous intolerance to oral administration, severe exacerbation or who have poor perfusion secondary to shock.

The efficacy of inhaled corticosteroids in exacerbation of COPD has not been studied; therefore they should not be used in place of oral corticosteroids in this population. In addition, the bioavailability of oral and intravenous corticosteroids is about equal, and there is less risk (extravasation, phlebitis, etc.) with oral versus intravenous administration. Although not commonly used in the prehospital environment, corticosteroids can be safely administered in the prehospital setting.

In summary, treatment for the patient in Case #1 should consist of:

• Administration of oxygen via nasal cannula at 1 lpm;

• Administration of nebulized short-acting beta agonists and nebulized anticholinergics. If 100% oxygen is used to power the nebulizer, consider limiting nebulizer treatment to six minutes to prevent overoxygenation;

• IV access and cardiac monitoring during transport.

Case #2

A 62-year-old male presents conscious, alert and oriented times four, sitting on a chair in his living room in obvious respiratory distress, complaining of difficulty breathing. He describes a four-day history of general malaise, low-grade fever and increased cough and sputum production. His difficulty breathing started about two days ago and has gotten worse since. He denies any chest pain or discomfort, nausea or vomiting, dizziness, weakness, syncope or abdominal, head or back pain. He has a history of COPD and is prescribed Combivent MDI prn; Foradil MDI bid; and Spiriva MDI bid, though he says he ran out of Combivent last week and hasn’t been able to refill his prescription. He is on home oxygen via nasal cannula at 2 lpm.

When asked he tells you his last COPD exacerbation occurred 18 months ago and required a three-day hospitalization for treatment of pneumonia. He did not require intubation but was sent home on a two-week corticosteroid regimen. You note that the patient is tripoding, in the sniffing position and breathing through pursed lips with a prolonged expiratory phase. He is able to speak in 2–3-word sentences. Your clinical exam reveals inspiratory and expiratory wheezes in all lung fields with heavy rhonchi in the upper right lung field. There is no JVD or peripheral edema, and his skin is warm and dry with poor turgor. His mucus membranes are dry. His vital signs are: HR, 96/min. and irregular; BP, 132/74 mmHg; RR, 20/min. with good tidal volume and prolonged expiratory phase; SpO₂, 80% on room air; EtCO₂, 72 mmHg with a “shark fin” waveform morphology. A 12-lead ECG reveals atrial fibrillation with occasional unifocal PVCs.

What is your differential diagnosis? What are the important clinical and historical findings? How would you manage this patient?

Discussion

The patient’s HPI of general malaise, low-grade fever, increased cough and sputum production and the heavy rhonchi in the upper right lobe strongly suggests pneumonia as the cause of his COPD exacerbation. It is estimated that up to 80% of COPD exacerbations occur secondary to bacterial or viral respiratory infection.¹³ In addition, the “shark fin” capnography waveform morphology is consistent with bronchoconstriction, which would not be consistent with pneumothorax, PE or CHF as a primary cause of the respiratory distress.

As in Case #1, this patient’s medications offer some insight to the severity of his disease. He is prescribed a short-acting bronchodilator, Combivent (albuterol/ipratropium), a long-acting beta agonist, Foradil (formoterol), and a long-acting anticholinergic, Spiriva (tiotropium). This prescribing of a combination (beta agonist and anticholinergic) short-acting bronchodilator used when needed and regular treatment with a long-acting beta agonist and long-acting anticholinergic indicates he is considered high-risk for exacerbations yet is less symptomatic than others in this high-risk category at baseline in the GOLD Therapy by Disease Category Severity recommendations.¹

The patient’s COPD history offers additional insight. Important factors to inquire about include the number and frequency of prior exacerbations, exacerbations requiring treatment with systemic corticosteroids and/or antibiotics, exacerbations requiring hospitalization, and previous need for intubation and/or ventilatory support—all important factors in determining the likelihood of severe exacerbation.¹

The patients in both cases presented with atrial fibrillation, and the patient in Case #2 also had frequent unifocal PVCs. Patients with COPD are at increased risk for atrial dysrhythmias such as atrial fibrillation and multifocal atrial tachycardia, as well as ventricular dysrhythmias.¹⁴ Chronic hypoxia and acidosis, theophylline and beta agonist use, and comorbidities such as coronary artery disease, hypertension and electrolyte disturbances and other factors contribute to the occurrence of cardiac dysrhythmias in this population.¹⁵

There is ample clinical evidence to show this patient is in respiratory distress and would benefit from ventilatory support. He is tripoding and assuming a sniffing position to maximize upper airway airflow, and is pursed-lipped breathing with a prolonged expiratory phase. Pursed-lipped breathing, a clinical exam finding uniquely associated with COPD, creates physiologic positive end-expiratory pressure (PEEP) to keep the lower airways open to ventilate more effectively. The prolonged expiratory phase allows for a more complete ventilation of the alveoli. The EtCO₂ of 72 mmHg is high, suggesting the patient is having trouble ventilating effectively.

If available, initiate noninvasive positive-pressure ventilation (NPPV) to help reduce the work of breathing and improve alveolar ventilation. When used in the setting of COPD exacerbation, NPPV has been shown to improve respiratory acidosis, decrease the work of breathing and decrease length of hospital stay. Perhaps most important, NPPV reduces mortality and the need for intubation.¹ Patients with severe exacerbations of COPD respond to NPPV better than those with less serious exacerbations.¹⁶

Options for NPPV in the prehospital setting commonly include bilevel positive airway pressure (BiPAP) and continuous positive airway pressure (CPAP). Both methods will effectively accomplish what the patient is attempting to produce with his pursed-lipped breathing: an elevated airway pressure to open the lower airways and increase ventilation. BiPAP is less common in the prehospital setting, as it requires the use of a mechanical ventilator, an expensive piece of equipment that requires significant training to use safely and effectively. BiPAP delivers preset inspiratory and expiratory positive airway pressures.

CPAP delivers a preset constant pressure to the airways and is functionally similar to PEEP. Unlike BiPAP, inspiratory and expiratory pressures are the same. Disposable CPAP units are commonly found in the prehospital setting due to their lower cost and ease of use compared to BiPAP units. Many CPAP devices found in the prehospital setting operate using 100% oxygen via a high-pressure DISS port or regular flow rate to create the pressures required to operate. While some CPAP units allow for the adjusting of FiO₂ via a Venturi valve, many designed for prehospital use lack the ability to adjust and therefore provide close to 100% FiO₂, depending on the fit of the mask. As previously discussed, this is not ideal in the patient with COPD. If possible, the FiO₂ and/or flow rate should be adjusted as needed to maintain an SpO₂ of 88%–92%. If the NPPV device allows for the piggybacking of a nebulizer, bronchodilators should be administered and the patient’s EtCO₂ and capnograph waveform morphology monitored to gauge effectiveness.

In the absence of CPAP or BiPAP, administer oxygen and bronchodilators via nebulizer with oxygen administration titrated as possible to achieve an SpO₂ of 88%–92%.

In summary, treatment for the patient in Case #2 should consist of:

• NPPV via CPAP or BiPAP;

• Oxygen administration titrated to achieve an SPO₂ of 88%–92%;

• Bronchodilators via nebulizer;

• IV access and cardiac monitoring during transport.

Case #3

An 83-year-old female presents lethargic and confused, slumped on a couch in severe respiratory distress. Her husband says she’s had a chest cold for the past two days and started experiencing shortness of breath yesterday that got worse over the past 24 hours. He also describes increased sputum production, and you note a trash can next to the couch overflowing with sputum-soaked tissues. “She was up all night breathing hard, using her inhalers,” he reports. Her breathing became much worse over the past hour, and he called 9-1-1 “when she couldn’t even sit up anymore.”

You note she’s alert but confused to place, time and event. Her skin is cool, cyanotic and slightly moist, she’s using accessory muscles to assist breathing, and her respirations are slow and shallow. Her husband says she has a history of COPD, type 2 diabetes mellitus, osteoporosis and cardiovascular disease, with a heart attack two years prior. Her medications include levalbuterol MDI; ipratropium MDI; Flovent MDI; Serevent MDI; Daliresp; theophylline; ASA; nitroglycerin; and Glucotrol. The husband also describes a history of many exacerbations of the patient’s COPD over the past two years, with “four or five” visits to the ED, three hospitalizations with intubation, and home corticosteroid and antibiotic use.

Your clinical exam reveals very little air movement in all fields with diffuse inspiratory and expiratory wheezes and lung sounds diminished in all fields. Her vital signs are: HR, 130/min. and irregular; BP, 108/54 mmHg; RR, 8/min. and shallow; SpO₂, 61% on room air; EtCO₂, 80 mmHg with a “shark fin” waveform morphology. A 12-lead ECG reveals multifocal atrial tachycardia with frequent multifocal PVCs, and a 12-lead ECG shows no acute ST-segment changes.

Discussion

This patient is in respiratory failure, as evidenced by her lethargy, altered mental status, slow and shallow breathing, hypoxia and hypercapnea. Unfortunately she is not a candidate for NPPV, as she has an altered mental status and is not breathing adequately. As such, endotracheal intubation is required.

The decision to intubate a patient in respiratory distress secondary to COPD exacerbation should not be made without careful consideration of other options such as NPPV, as endotracheal intubation and mechanical ventilation for COPD patients is associated with longer ICU stays and higher rates of ICU mortality compared to COPD patients not intubated and ventilated mechanically. In addition, successful weaning of a patient off mechanical ventilation is often difficult and hazardous.

If you decide to intubate a patient with severe COPD exacerbation, the usual precautions regarding overoxygenation in this population need not be considered. It’s OK, and in fact prudent, to hyperoxygenate these patients prior to intubation. The patient should be preoxygenated prior to the intubation attempt with CPAP or a bag-mask device with PEEP, and apneic oxygenation provided via nasal cannula during the intubation attempt. This will ensure the highest SpO₂ possible and delay the onset, or at least the severity, of hypoxia during the intubation attempt. Remember, patients with COPD are chronic CO₂ retainers and have a shallow oxygen reserve and can be anticipated to desaturate more quickly than patients without COPD. Adequate preoxygenation prior to intubation is vitally important. After successful intubation, the previously discussed target SpO₂ of 88%–92% can be maintained.

Whether an intubated patient is ventilated manually with a BVM or with a mechanical ventilator, take care to ensure a full exhalation is allowed between ventilations to prevent ventilator-induced dynamic hyperinflation, or “breath stacking.” This occurs when a ventilation is initiated prior to the previous exhalation finishing. In patients with severe COPD exacerbation, severe airflow limitation prevents total exhalation, resulting in an increased end-expiratory volume in the lungs. With each additional breath, “breath stacking” occurs, gradually increasing the residual volume and pressure within the lungs and chest, putting the patient at risk for barotrauma and the hemodynamic instability and cardiovascular collapse that can occur with increased intrathoracic pressure. Allowing for a prolonged expiratory time is vital in patients with severe COPD exacerbation. This can be achieved by decreasing the respiratory rate and/or tidal volume (and subsequently minute volume), and in patients receiving mechanical ventilation increasing inspiratory flow rate to 60–100 mL/ min.

In addition to intubation and positive-pressure ventilation, this patient should receive nebulized bronchodilators to reverse bronchoconstriction. If available, IV corticosteroids would be indicated as well. Magnesium sulfate, widely used in the prehospital setting in the treatment of severe asthma, is not as widely used in acute COPD exacerbation, nor has it been extensively studied (see sidebar).

This patient had a number of comorbidities associated with COPD, including cardiovascular disease, osteoporosis, diabetes and depression. These comorbidities have a severe negative impact on the prognosis of the COPD patient and can give the caregiver information regarding the most likely course of a patient’s condition during treatment and transport.

This patient’s COPD history can also indicate her probable course of events. She has a history significant for multiple visits to the ED, hospital admissions, ICU stays and intubations, all of which suggest this exacerbation will most likely not respond favorably to prehospital intervention and will require aggressive management in the ED as well as admission to an ICU.

In addition to the history, the patient’s medications hint at the severity of her COPD. She has been prescribed a short-acting beta agonist (levalbuterol), a short-acting anticholenergic (ipratropium), an inhaled glucocorticoid (Flovent/fluticasone), a long-acting beta agonist (Serevent/salmeterol), a phosphodiesterase-4 inhibitor (Daliresp/roflumilast), as well as a methylxanthine (theophylline). This medication regimen indicates she is considered high-risk for exacerbations and is more symptomatic than others in this category at baseline in the GOLD Therapy by Disease Category Severity recommendations.¹

The patient presented with multifocal atrial tachycardia on ECG, a common dysrhythmia associated with COPD as well as theophylline use. Theophylline has many well-documented cardiac effects, such as increases in heart rate (which is directly related to serum theophylline levels) and atrial dysrhythmias such as atrial fibrillation, multifocal atrial tachycardia and ventricular dysrhythmias. In our patient in Case #3, the frequent multifocal PVCs should not be treated with antidysrhythmics but should be treated indirectly by correcting hypoxia.

In summary, treatment for the patient in Case #3 should consist of:

• BVM ventilation and preoxygenation;

• Endotracheal intubation with BVM or mechanical ventilation. Reduce rate and/or tidal volume and inspiratory flow rates to prevent dynamic hyperinflation;

• Administration of nebulized bronchodilators;

• Administration of IV corticosteroids if available;

• IV access and cardiac monitoring.

Conclusion

The mainstays of the treatment of exacerbation of COPD in the prehospital setting include:

• Ensuring adequate ventilation and oxygenation (SpO₂ 88%–92%);

• In intubated patients, adjusting minute volume and inspiratory flow rates when possible to prevent dynamic hyperinflation;

• Administration of nebulized bronchodilators;

• IV access and cardiac monitoring.

In addition, obtaining a thorough, detailed and accurate history can help the provider anticipate likely outcomes and responses to prehospital treatment, allowing for a better overall understanding of the evolving situation.

References

1. Global Initiative for Chronic Obstructive Lung Disease. Global strategy for the diagnosis, management, and prevention of COPD, www.goldcopd.org/guidelines-global-strategy-for-diagnosis-management.html.

2. Weiss ST. Chronic obstructive pulmonary disease: Prognostic factors and comorbid conditions. UpToDate.com, www.uptodate.com/contents/chronic-obstructive-pulmonary-disease-prognostic-factors-and-comorbid-conditions.

3. Hoyert DL, Xu JQ. Deaths: preliminary data for 2011. Natl Vital Stat Rep, 2012; 61(6): 1–65.

4. Lopez AD, Shibuya K. Chronic obstructive pulmonary disease: current burden and future projections. Eur Respir J, 2006; 27(2): 397.

5. Centers for Disease Control and Prevention. Chronic obstructive pulmonary disease among adults—United States, 2011. MMWR, 2012; 61(46): 938–43.

6. Mannino DM, Gagnon RC, Petty TL, Lydick E. Obstructive lung disease and low lung function in adults in the United States: data from the National Health and Nutrition Examination Survey 1988–1994. Arch Intern Med, 2000; 160: 1,683-9.

7. Centers for Disease Control and Prevention. What is COPD?, www.cdc.gov/copd/index.htm.

8. Stoller JK. Management of exacerbations of chronic obstructive pulmonary disease. UpToDate.com, www.uptodate.com/contents/management-of-exacerbations-of-chronic-obstructive-pulmonary-disease.

9. Light RW. Secondary spontaneous pneumothorax in adults. UpToDate.com, https://www.uptodate.com/contents/secondary-spontaneous-pneumothorax-in-adults.

10. Austin MA, Willis KE, et al. Effect of high flow oxygen on mortality in chronic obstructive pulmonary disease patients in prehospital setting: randomized control trial. BMJ, 2010 Oct 18; 341: c5,462.

11. Ntoumenopoulos G. Using titrated oxygen instead of high flow oxygen during an acute exacerbation of chronic obstructive pulmonary disease (COPD) saves lives. J Physiother, 2011; 57(1): 55.

12. O’Driscoll BR, Howard LS, Davison AG. BTS guideline for emergency oxygen use in adult patients. Thorax, 2008; 63: vi1–68.

13. Sapey E, Stockley RA. COPD exacerbations 2: Aetiology. Thorax, 2006; 61: 250–8.

14. Sode BF, Dahl M, Nordestgaard BG. Myocardial infarction and other co-morbidities in patients with chronic obstructive pulmonary disease: a Danish nationwide study of 7.4 million individuals. Eur Heart J, 2011 Oct; 32(19): 2,365–75.

15. Minai OA. Arrhythmias in COPD. UpToDate.com, www.uptodate.com/contents/arrhythmias-in-copd.

16. Bauman KA, Hyzy RC. Noninvasive positive pressure ventilation in acute respiratory failure in adults. UpToDate.com, https://www.uptodate.com/contents/noninvasive-positive-pressure-ventilation-in-acute-respiratory-failure-in-adults.

17. Shivanthan MC, Rajapaske S. Magnesium for acute exacerbation of chronic obstructive pulmonary disease: A systematic review of randomised trials. Ann Thorac Med, 2014 Apr; 9(2): 77–80.

Scott R. Snyder, BS, NREMT-P, is full-time faculty at the Public Safety Training Center in the Emergency Care Program at Santa Rosa Junior College, CA. He is also a paramedic with AMR: Sonoma Life Support in Santa Rosa, CA. E-mail scottrsnyder@me.com.

Sean M. Kivlehan, MD, MPH, NREMT-P, is an emergency medicine resident at the University of California, San Francisco. E-mail sean.kivlehan@gmail.com.

Kevin T. Collopy, BA, FP-C, CCEMT-P, NREMT-P, WEMT, is clinical education coordinator for VitaLink/AirLink in Wilmington, NC, and a lead instructor for Wilderness Medical Associates. E-mail ktcollopy@gmail.com.